Linked Life Data

1415539

Source:http://linkedlifedata.com/resource/pubmed/id/1415539

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3 Pt 1
pubmed:dateCreated
1992-10-29
pubmed:abstractText
To assess whether prolonged intrauterine stress and resultant fetal growth retardation result in depletion of adrenal catecholamines and alter the adrenergic signal transduction system, we studied newborn sheep after single umbilical artery ligation (SUAL)-induced growth retardation. The animals were delivered at term, and postnatal cardiovascular, pulmonary, endocrine, and metabolic responses were measured. We also evaluated the status of myocardial and pulmonary beta-adrenergic receptor number and function. SUAL caused significant growth retardation but relative preservation of brain and adrenal gland weight and adrenal catecholamine content. Blood pressure, plasma free fatty acid, and glucose responses at birth were blunted in SUAL animals. The plasma epinephrine (Epi) and norepinephrine levels were comparable in both groups for the first 2 h of age. By 4 h, both plasma concentration and plasma appearance rate of Epi were reduced to 40% of control in SUAL animals (P less than 0.05). Neither beta-receptor density, affinity, nor adenylate cyclase activity were altered by SUAL in either cardiac or pulmonary membranes. These results suggest that, rather than overt depletion, there is relative sparing of initial adrenal medullary function that later waned. This response and preservation of the beta-adrenergic signal transduction system may represent partial compensation for the physiological stress induced by SUAL.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0002-9513
pubmed:author
pubmed:issnType
Print
pubmed:volume
263
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
E575-83
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed:year
1992
pubmed:articleTitle
Single umbilical artery ligation-induced fetal growth retardation: effect on postnatal adaptation.
pubmed:affiliation
Perinatal Research Laboratories, University of California Los Angeles School of Medicine, Torrance 90509.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't